English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
  Mechanisms of mitochondria and autophagy crosstalk

Rambold, A., & Lippincott-Schwarz, J. (2011). Mechanisms of mitochondria and autophagy crosstalk. Cell Cycle, 10, 4032-4038. doi:10.4161/cc.10.23.18384.

Item is

Basic

show hide
Item Permalink: http://hdl.handle.net/21.11116/0000-0005-C441-4 Version Permalink: http://hdl.handle.net/21.11116/0000-0005-C442-3
Genre: Journal Article

Files

show Files
hide Files
:
Rambold et al..pdf (Publisher version), 2MB
Name:
Rambold et al..pdf
Description:
-
Visibility:
Public
MIME-Type / Checksum:
application/pdf / [MD5]
Technical Metadata:
Copyright Date:
-
Copyright Info:
-
License:
-

Locators

show
hide
Description:
-

Creators

show
hide
 Creators:
Rambold, Angelika1, Author              
Lippincott-Schwarz, J.2, Author
Affiliations:
1Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243650              
2External Organizations, ou_persistent22              

Content

show
hide
Free keywords: -
 Abstract: Autophagy is a cellular survival pathway that recycles intracellular components to compensate for nutrient depletion and ensures the appropriate degradation of organelles. Mitochondrial number and health are regulated by mitophagy, a process by which excessive or damaged mitochondria are subjected to autophagic degradation. Autophagy is thus a key determinant for mitochondrial health and proper cell function. Mitophagic malfunction has been recently proposed to contribute to progressive neuronal loss in Parkinson's disease. In addition to autophagy's significance in mitochondrial integrity, several lines of evidence suggest that mitochondria can also substantially influence the autophagic process. The mitochondria's ability to influence and be influenced by autophagy places both elements (mitochondria and autophagy) in a unique position where defects in one or the other system could increase the risk to various metabolic and autophagic related diseases.

Details

show
hide
Language(s): eng - English
 Dates: 2011
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.4161/cc.10.23.18384
 Degree: -

Event

show

Legal Case

show

Project information

show

Source 1

show
hide
Title: Cell Cycle
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: Georgetown, TX : Landes Bioscience
Pages: - Volume / Issue: 10 Sequence Number: - Start / End Page: 4032 - 4038 Identifier: ISSN: 1538-4101
CoNE: https://pure.mpg.de/cone/journals/resource/111088196488836